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UPR-RCM SRNA PHARM I > Chapter 11: Neuromuscular Physiology > Flashcards

Chapter 11: Neuromuscular Physiology Flashcards

1
Q

How does acetylcholine interact with nicotinic acetylcholine receptors (nAChRs)?

A
  1. Acetylcholine binds to the α subunits of the nAChRs.
  2. Binding occurs when two acetylcholine molecules cooperatively attach to sites on the extracellular surface of the receptor.
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2
Q

What triggers the opening of ligand-gated cation channels at the neuromuscular junction (NMJ)?

A
  • The channels open almost instantaneously when two acetylcholine molecules bind to the nAChRs, causing a conformational shift in the subunits.
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3
Q

What happens at the cellular level when acetylcholine binds to nAChRs?

A
  • Sodium ions flow down their electrochemical gradient into the muscle cell, depolarizing the muscle cell membrane at the NMJ.
  • Simultaneously, potassium exits the cytosol of the muscle fiber.
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4
Q

What is the effect of depolarization on voltage-gated calcium ion channels in the motor nerve?

A
  • Opens voltage-gated calcium ion channels, which triggers the mobilization of synaptic vesicles (SVs)
  • Activates the fusion machinery in the nerve terminal, leading to the release of acetylcholine.
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5
Q

What is the function of potassium channels in the nerve terminal during neurotransmitter release?

A
  • Limit the extent of calcium ion entry and neurotransmitter release.
  • They help initiate repolarization of the nerve terminal, thus regulating the process.
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6
Q

How does depolarization at the muscle membrane activate sodium channels?

A
  • Depolarization activates voltage-gated sodium channels present in the muscle membrane.
  • These channels mediate the initiation and propagation of action potentials across the muscle membrane.
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7
Q

What is the role of sodium channels in the muscle membrane regarding action potentials?

A
  • Are responsible for the upstroke of the action potential.
  • Facilitating its propagation across the muscle surface and into the transverse tubules (T tubules).
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8
Q

What are the two types of calcium channels involved in muscle contraction?

A
  • Dihydropyridine receptor (DHPR) in the T tubules and the
  • Ryanodine receptor 1 (RyR1) in the sarcoplasmic reticulum (SR).
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9
Q

What is the role of dihydropyridine receptors (DHPRs) in muscle contraction?

A
  • Act as “voltage sensors” and are activated by membrane depolarization.
  • Their activation, in turn, triggers the activation of RyR1 receptors.
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10
Q

What happens during the DHPR-RyR1 interaction in muscle cells?

A
  • Releases large amounts of calcium ion from the sarcoplasmic reticulum (SR).
  • Leading to a transient increase in myoplasmic free calcium ion concentration.
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11
Q

How does calcium ion contribute to muscle contraction?

A
  • The increased myoplasmic calcium ion binds to troponin C, initiating the movement of tropomyosin on the thin filament (actin).
  • This allows cross-bridges to form between myosin and actin, resulting in force development, a process known as excitation-contraction coupling.
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12
Q

What role does the calcium ion pump play in muscle relaxation?

A
  • The calcium ion pump in the SR actively reaccumulates calcium ions, lowering their concentration in the sarcoplasm.
  • This process, powered by ATP, stops cross-bridging between myosin and actin, leading to muscle relaxation.
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13
Q

What is the consequence of the failure of the calcium ion pump in skeletal muscles?

A
  • Results in sustained skeletal muscle contraction
  • Increased heat production, leading to malignant hyperthermia.
  • The RyR1 gene, associated with malignant hyperthermia susceptibility, is located on chromosome 19.
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14
Q

How is repolarization of the muscle membrane initiated?

A
  • Begins with the closing of sodium channels and the opening of potassium (K+) channels, which conduct an outward K+ current.
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15
Q

How does the muscle membrane potential return to its resting level?

A
  • The muscle membrane potential returns to its resting level (approximately −70 to −90 mV)
  • By allowing chloride (Cl−) ions to enter the cell through voltage-sensitive chloride channels.
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16
Q

How much can skeletal muscle blood flow increase during strenuous exercise?

A
  • More than 20 times during strenuous exercise,
  • The greatest increase of any tissue in the body.
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17
Q

What percentage of capillaries are open in skeletal muscles at rest, and how does this change during exercise?

A
  • At rest, only 20% to 25% of the capillaries in skeletal muscles are open.
  • During strenuous exercise, almost all capillaries become patent.
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18
Q

What are the benefits of opening previously collapsed capillaries in muscles during exercise?

A
  • Reduces the diffusion distance for oxygen and nutrients to skeletal muscle fibers.
  • Increases the surface area for nutrient diffusion.
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19
Q

What causes vasodilation in skeletal muscles during exercise?

A
  • Exercise reduces local oxygen concentration, leading to vasodilation.
  • Possibly due to the vessel walls’ inability to maintain contraction without oxygen or the release of vasodilators like K+ and adenosine.
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20
Q

How does exercise affect cardiac output?

A
  • The increase in cardiac output during exercise is mainly due to local vasodilation in active skeletal muscles
  • Increased venous return to the heart.
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21
Q

What is the effect of exercise on the sympathetic nervous system and systemic blood pressure?

A
  • Triggers a centrally mediated sympathetic response, causing vasoconstriction in nonmuscular tissues
  • Increases in systemic blood pressure, but excessive pressure increases are moderated by vasodilation in skeletal muscles.
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22
Q

Which circulations are exceptions to the nonmuscular tissue vasoconstriction induced by exercise?

A
  • Thecoronary and cerebral circulationsare exceptions
  • They do not undergo vasoconstriction during exercise, vital for the response to exercise along with skeletal muscles.
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23
Q

What role does the calcium ion pump play in muscle relaxation?

A
  • The calcium ion pump in the SR actively reaccumulates calcium ions, lowering their concentration in the sarcoplasm.
  • This process, powered by ATP, stops cross-bridging between myosin and actin, leading to muscle relaxation.
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24
Q

How is smooth muscle anatomically distinguished from skeletal and cardiac muscle?

A
  • Smooth muscle lacks visible cross-striations as actin and myosin are not arranged in regular arrays.
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25
Q

What are the two categories of smooth muscle?

A
  • Multiunit
  • Visceral smooth muscle.
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26
Q

What characterizes multiunit smooth muscle?

A
  • Multiunit smooth muscle contraction is controlled almost exclusively by nerve signals, with spontaneous contractions being rare.
  • Examples include the ciliary muscles of the eye and smooth muscles of many large blood vessels.
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27
Q

How do calcium ions enter smooth muscle cells?

A
  • In smooth muscle, the sarcolemma contains caveoli, which are saclike inpocketings where calcium ions may enter through voltage-gated calcium ion channels.
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28
Q

What types of calcium ion channels are found in the sarcoplasmic reticulum (SR) of smooth muscles?

A
  • RyR1 channels (similar to skeletal muscles)
  • Inositol 1,4,5-triphosphate (IP3)-gated calcium ion channels.
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29
Q

What is unique about visceral smooth muscle?

A
  • Visceral smooth muscle often forms a functional syncytium
  • undergoes spontaneous contractions as a single unit
  • particularly prominent in tubular structures for peristaltic motion.
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30
Q

What is notable about the action potentials in visceral smooth muscle?

A
  • Visceral smooth muscle can have plateaus in action potentials lasting up to 30 seconds, especially in the ureters and uterus, with a resting transmembrane potential of approximately −60 mV.
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31
Q

How does smooth muscle respond to hormones and local tissue factors?

A
  • Uniquely sensitive to hormones and local factors, which
  • Can cause contraction by activating calcium ion transport or
  • Relax the muscle by increasing cyclic adenosine or guanosine monophosphate.
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32
Q

What proteins are involved in smooth muscle contraction, and how do they differ from skeletal muscle?

A
  • Smooth muscles contain actin and myosin.
  • Skeletal muscles, they lack troponin and are innervated by autonomic neurons.
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33
Q

How does the calcium-calmodulin complex contribute to smooth muscle contraction?

A
  • The calcium-calmodulin complex activates the enzyme necessary for phosphorylation of myosin
  • Leading to actin sliding on myosin and producing contraction.
34
Q

What is the primary source of calcium in smooth muscle contraction?

A

Comes from extracellular fluid during action potentials, as the SR in smooth muscle is poorly developed.

35
Q

How does the duration of smooth muscle contraction compare to that of skeletal muscle?

A
  • The duration of smooth muscle contraction is often seconds, much longer than skeletal muscle contractions
  • Due to the slow calcium ion transport system.
36
Q

What happens to smooth muscles when they are denervated?

A
  • Smooth muscles do not atrophy when denervated but become hyperresponsive to normal neurotransmitters
  • due to the synthesis or activation of more receptors.
37
Q

Describe the arrangement of nerve fibers in smooth muscle.

A
  • In smooth muscle, nerve fibers branch diffusely over the muscle fibers without making actual contact.
  • secreting neurotransmitters into the interstitial fluid.
38
Q

How do acetylcholine and norepinephrine function in smooth muscle?

A
  • Acetylcholine can be excitatory or inhibitory in smooth muscles, depending on the site.
  • Norepinephrine often exerts the opposite effect.
39
Q

What characterizes the electrical and contractile activity of uterine smooth muscle?

A
  • Uterine smooth muscle exhibits a high degree of spontaneous electrical and contractile activity
  • with contractions spreading from cell to cell at a rate of 1 to 3 cm/s.
40
Q

What are the peak intrauterine pressures during the second stage of labor?

A
  • Peak intrauterine pressures can reach 60 to 80 mm Hg.
  • Resting uterine pressure is approximately 10 mm Hg.
41
Q

What ion movement is key in uterine depolarization and contraction?

A
  • Sodium ion movement is the primary determinant in depolarization of the uterine smooth muscle.
  • Calcium ions are necessary for excitation-contraction coupling.
42
Q

How does calcium ion availability influence uterine smooth muscle?

A
  • Influences the response of uterine smooth muscle to both physiological and pharmacological stimuli.
43
Q

What types of receptors are present in uterine smooth muscle (myometrium)?

A
  • α excitatory receptors
  • β inhibitory receptors.
44
Q

What are the components of the Neuromuscular Junction (NMJ)?

A
  • Motor neuron
  • Muscle fiber
  • Schwann cells.
45
Q

How does innervation at the NMJ change postnatally?

A
  • Initially, muscle fibers are innervated by multiple motor nerves.
  • This transitions to single innervation within a few days postnatally.
46
Q

Describe the structure of motor nerve endings at the NMJ.

A
  • The motor nerve ending branches and invaginates into the skeletal muscle fiber outside the sarcolemma.
  • Schwann cells cap the naked motor nerve terminals not in contact with the muscle fiber.
47
Q

What are the structural components of the NMJ?

A
  1. Presynaptic nerve terminal (with synaptic vesicles and mitochondria)
  2. The synaptic cleft (with basal lamina and acetylcholinesterase)
  3. The postsynaptic muscle membrane (with infoldings.)
48
Q

Where are nAChRs located at the NMJ, and what is their function?

A
  • nAChRs are concentrated at the crests of secondary folds of the postsynaptic muscle membrane.
  • Directly opposing the active zones of the presynaptic membrane.
49
Q

What factors contribute to the plasticity of neuromuscular transmission?

A
  • Involves the synthesis, storage, and release of acetylcholine, binding of acetylcholine to nicotinic receptors and action potential generation,
  • Rapid hydrolysis of acetylcholine, and adaptation of muscle contractile proteins
50
Q

How is synaptic plasticity defined?

A
  • Is the ability of individual synaptic junctions to change in strength in response to either use or disuse.
51
Q

How are synaptic vesicles (SVs) formed and transported to the nerve terminal?

A
  • SVs are synthesized in the neuronal cell body within the endoplasmic reticulum
  • Transported to the nerve terminal via the microtubule system.
52
Q

How is acetylcholine loaded into SVs?

A
  • Acetylcholine is synthesized from acetyl coenzyme A and choline.
  • Then an energy-dependent transporter accumulates it within the vesicles, each containing 5,000 to 10,000 molecules.
53
Q

What does a “quantum” of transmitter refer to in the context of SVs?

A
  • Refers to the acetylcholine contained in a single vesicle.
54
Q

What types of proteins are found in synaptic vesicles?

A
  • Synaptic vesicles possess transport proteins for neurotransmitter uptake
  • Proteins that mediate SV membrane traffic such as docking, fusion, and budding.
55
Q

What are the two pools of vesicles in the nerve terminal?

A
  1. There are two vesicle pools: a readily releasable store (active pool)
  2. Reserve store. The active pool is aligned near the active zones.
56
Q

What is the miniature endplate potential?

A
  • Represents the depolarization produced by the contents of a single vesicle on the postsynaptic membrane.
57
Q

How is the endplate potential generated?

A
  • Results from the summation of miniature endplate potentials produced by the acetylcholine from fewer than 50 to 300 SVs.
58
Q

What happens to acetylcholine after it is released from SVs?

A
  • About 50% of released acetylcholine is hydrolyzed by acetylcholinesterase during diffusion across the synaptic cleft.
  • Choline, a product of this hydrolysis, is recycled back into the terminal for acetylcholine resynthesis.
59
Q

What is the synaptic cleft and its size?

A
  • The synaptic cleft is a space less than 20 to 50 nm wide, separating nerve and muscle fiber plasma membranes.
  • Encompasses the synaptic basal lamina, and filled with extracellular fluid.
60
Q

What is the role of acetylcholinesterase at the synaptic cleft?

A
  • Acetylcholinesterase, bound to the basal lamina at the cleft.
  • Catalyzes the hydrolysis of acetylcholine, processing about 4,000 molecules per active site per second.
61
Q

How efficient is acetylcholinesterase and where is it concentrated?

A
  • Acetylcholinesterase is one of the most efficient catalytic enzymes.
  • Is highly concentrated at the NMJ, with lower concentrations along muscle fibers.
62
Q

Besides hydrolyzing acetylcholine, what other functions does acetylcholinesterase have?

A
  • Has nerve growth-promoting activities.
  • Modulates nicotinic acetylcholine receptors (nAChRs).
63
Q

What factors regulate acetylcholinesterase?

A
  • Is regulated by muscle activity and plasma membrane depolarization.
  • Its density decreases significantly after denervation.
64
Q

What is the structure and concentration of nAChRs in adult skeletal muscle?

A
  • nAChRs are pentameric complexes concentrated at over 10,000 per μm² on the crests of junctional folds.
  • Each with two α subunits and single β, δ, and ε subunits forming a transmembrane pore.
65
Q

How do fetal and adult nAChRs differ?

A
  • Fetal nAChRs contain a γ subunit instead of an ε subunit.
  • Have a low conductance channel, shorter burst duration.
  • Higher conductance to Na+, K+, and Ca2+ than adult nAChRs.
66
Q

How does acetylcholine binding to nAChRs initiate channel opening?

A
  • Binding of two acetylcholine molecules to the α subunits of nAChRs causes conformational changes, opening a channel for Na+ and Ca2+ influx and K+ efflux.
67
Q

How do nondepolarizing neuromuscular-blocking drugs affect nAChRs?

A
  • These drugs bind to one or both α subunits of nAChRs but lack agonist activity, preventing conformational changes.
  • keeping the receptor channel closed, blocking neuromuscular transmission.
68
Q

What is the effect of succinylcholine on nAChRs

A
  • Succinylcholine, a partial agonist.
  • Binds to the α subunit and opens ion channels.
  • Causing a depolarizing block due to its prolonged channel opening as it is not hydrolyzed by acetylcholinesterase.
69
Q

What happens when large doses of nondepolarizing neuromuscular-blocking drugs are used?

A
  • High doses may enter nAChR channels, blocking ion flow and causing a blockade similar to that produced by local anesthetics on sodium ion channels.
70
Q

Where do α motor neurons originate and how do they reach skeletal muscles?

A
  • α Motor neurons originate from cell bodies in the brainstem or ventral horns of the spinal cord.
  • Reach muscles through mixed peripheral nerves, with each nerve terminal innervating a single muscle cell.
71
Q

What composes a motor unit?

A
  • A single myelinated α motor neuron and all muscle fibers innervated by that neuron.
72
Q

How do motor units vary in size and function?

A
  • Larger motor nerves innervate more muscle fibers than smaller ones.
  • Small units typically innervate red slow muscle fibers, while large units innervate white or pale fast muscle fibers.
73
Q

What are the characteristics of red and white muscle fibers?

A
  • Red muscle fibers (e.g., masseters) have high myoglobin, mitochondria, and capillary content and are resistant to fatigue.
  • White muscle fibers (e.g., psoas muscle) have lesser such contents.
74
Q

How does muscle fiber composition relate to muscle function?

A
  • Muscles contain a mix of motor units, with the composition depending on their function.
  • This mix determines the overall characteristics and capabilities of the muscle.
75
Q

What are the three general classifications of muscle?

A
  • Muscle is classified as skeletal, smooth, or cardiac.
  • Both skeletal and cardiac muscles are striated, but they differ histologically and functionally.
76
Q

What are the differences between skeletal and cardiac muscle cells?

A
  • Skeletal muscle cells are multinucleated and tubular
  • Cardiac muscle cells may be mono- or binucleated, are branched, and contain intercalated discs.
77
Q

What are the primary functions of skeletal, smooth, and cardiac muscles?

A
  • Skeletal muscle is responsible for voluntary actions, whereas
  • Smooth and cardiac muscles are involved in cardiovascular, respiratory, gastrointestinal, and genitourinary system functions.
78
Q

What percentage of total body mass is composed of muscle?

A
  • Muscle composes 45% to 50% of total body mass,
  • Skeletal muscles accounting for about 40% of body mass.
79
Q

What is the specialization of muscle cells?

A
  • Muscle cells are specialized for the conversion of chemical energy into mechanical energy.
80
Q

How is smooth muscle activity related to certain illnesses?

A
  • Inappropriate activity of smooth muscle is involved in illnesses such as hypertension, atherosclerosis, asthma, and gastrointestinal disorders.

UPR-RCM SRNA PHARM I (7 decks)

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